Kwon Eun-Young, Lee Jeonghyeon, Kim Ye Jin, Do Ara, Choi Ji-Young, Cho Su-Jung, Jung Un Ju, Lee Mi-Kyung, Park Yong Bok, Choi Myung-Sook
Department of Food Science and Nutrition, Kyungpook National University, 1370 San-Kyuk Dong Puk-Ku, Daegu 41566, Korea.
Center for Food and Nutritional Genomics Research, Kyungpook National University, 1370 San-Kyuk Dong Puk-Ku, Daegu 41566, Korea.
Nutrients. 2017 Jun 2;9(6):569. doi: 10.3390/nu9060569.
The aim of the current study was to elucidate the effect of seabuckthorn leaves (SL) extract and flavonoid glycosides extract from seabuckthorn leaves (SLG) on diet-induced obesity and related metabolic disturbances, and additionally, to identify whether flavonoid glycosides and other components in SL can exert a possible interaction for the prevention of metabolic diseases by comparing the effect of SL and SLG. C57BL/6J mice were fed a normal diet (ND, AIN-93G purified diet), high-fat diet (HFD, 60 kcal% fat), HFD + 1.8% (/ SL (SL), and HFD + 0.04% (/) SLG (SLG) for 12 weeks. In high fat-fed mice, SL and SLG decreased the adiposity by suppressing lipogenesis in adipose tissue, while increasing the energy expenditure. SL and SLG also improved hepatic steatosis by suppressing hepatic lipogenesis and lipid absorption, whilst also enhancing hepatic fatty acid oxidation, which may be linked to the improvement in dyslipidemia. Moreover, SL and SLG improved insulin sensitivity by suppressing the levels of plasma GIP that were modulated by secreted resistin and pro-inflammatory cytokine, and hepatic glucogenic enzyme activities. SL, especially its flavonoid glycosides (SLG), can protect against the deleterious effects of diet-induced obesity (DIO) and its metabolic complications such as adiposity, dyslipidemia, inflammation, hepatic steatosis, and insulin resistance.
本研究的目的是阐明沙棘叶(SL)提取物和沙棘叶黄酮糖苷提取物(SLG)对饮食诱导的肥胖及相关代谢紊乱的影响,此外,通过比较SL和SLG的作用,确定SL中的黄酮糖苷和其他成分是否能在预防代谢疾病方面发挥可能的相互作用。将C57BL/6J小鼠分为四组,分别喂食正常饮食(ND,AIN-93G纯化饮食)、高脂饮食(HFD,脂肪含量60 kcal%)、HFD + 1.8%(/)SL(SL组)和HFD + 0.04%(/)SLG(SLG组),持续12周。在高脂喂养的小鼠中,SL和SLG通过抑制脂肪组织中的脂肪生成来降低肥胖程度,同时增加能量消耗。SL和SLG还通过抑制肝脏脂肪生成和脂质吸收来改善肝脂肪变性,同时增强肝脏脂肪酸氧化,这可能与血脂异常的改善有关。此外,SL和SLG通过抑制由分泌的抵抗素和促炎细胞因子调节的血浆GIP水平以及肝脏生糖酶活性来改善胰岛素敏感性。SL,尤其是其黄酮糖苷(SLG),可以预防饮食诱导的肥胖(DIO)及其代谢并发症,如肥胖、血脂异常、炎症、肝脂肪变性和胰岛素抵抗的有害影响。